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PubMed1985

The effect of desipramine upon melatonin and cortisol secretion in depressed and normal subjects.

Melatonin and cortisol values in plasma were measured hourly over 24 hours in six depressed patients and six normal volunteers before treatment and after one and three weeks of treatment with desipramine. The normal volunteers were further tested one week after withdrawal of desipramine. The mydriatic effects of tyramine and phenylephrine eye drops were also recorded in the normal volunteers. In neither group of subjects did desipramine treatment reduce melatonin secretion, suggesting that functionally significant down-regulation of beta andrenoceptors was not caused by this treatment. Melatonin secretion was significantly increased after three weeks of treatment in depressed patients. This increase was not found in normal subjects.

Adolescent↗

PubMed1989

A study of the effects of desipramine treatment alone and in combination with L-triiodothyronine on 6-sulphatoxymelatonin excretion in depressed patients.

Urinary 6-sulphatoxymelatonin (alpha MT6s) excretion was measured after one day and one, two and three weeks of desipramine treatment in eight depressed patients. There was significant increase in the urinary excretion of alpha MT6s after one week of treatment, and at no time was there any decrease in alpha MT6s excretion. These findings are opposed to the hypothesis that desipramine reduces noradrenergic neurotransmission in the human pineal. In a further five patients whose depression was resistant to desipramine alone, urinary alpha MT6s excretion was measured during treatment with adjunctive L-triiodothyronine (T3). There was no change in alpha MT6s excretion, and thus the previously reported potentiation of the efficacy of tricyclic antidepressants in combination with T3 does not appear to be mediated through an alteration in noradrenergic neurotransmission.

Adult↗

PubMed1993

REM sleep deprivation potentiates the effects of imipramine and desipramine but not that of clomipramine in the forced swimming test.

Effects of REM sleep (REMs) deprivation on the basal swimming activity and the tricyclic anti-depressants-induced increase in swimming activity in the forced swimming test were investigated. Immediately after a 48-hr period of REMs deprivation, the basal swimming activity in REMs-deprived mice was significantly higher than those in group-housed and socially isolated animals used as the control groups. The REMs deprivation-induced increase in the swimming activity was not changed by adrenoceptor antagonists and it returned to the control levels 3 hr after the REMs deprivation treatment. Moreover, imipramine and desipramine but not clomipramine further increased the swimming activity enhanced by REMs deprivation at doses that did not affect the activity in the control groups. The enhancing effect of REMs deprivation on the sensitivity to imipramine and desipramine remained unchanged even at 3 hr after the REMs deprivation treatment, and it was blocked by the alpha 2-adrenoceptor antagonist yohimbine. These results suggest that the REMs deprivation-induced increase in basal swimming activity in the forced swimming test is not mediated by adrenoceptor mechanisms, whereas the enhancing effect of REMs deprivation on the sensitivity to imipramine and desipramine may be mediated by the functional changes in alpha 2-adrenoceptors in the brain.

Adrenergic alpha-Antagonists↗

PubMed1994

Impact of desipramine or carbamazepine on patient retention in outpatient cocaine treatment: preliminary findings.

This is a preliminary report of a double-blind comparison of desipramine or carbamazepine to placebo among subjects participating in an outpatient cocaine treatment program. Sixty-five subjects were randomly assigned to one of the active drugs or placebo and followed until treatment completion or drop-out to determine if either drug enhanced retention in treatment and/or increased cocaine abstinence. There was no significant difference between carbamazepine or desipramine and placebo on either outcome measure in this preliminary analysis. While this is a preliminary report and does not take into account the heterogeneity of the patients in cocaine treatment, the results are consistent with those of other investigators and suggest that use of desipramine or carbamazepine may not offer any advantage in retaining cocaine-dependent patients in treatment.

Ambulatory Care↗

PubMed2006

Rates of in vivo methylation of desipramine and nortriptyline.

Routine monitoring of an 81-year-old man receiving treatment with nortriptyline for generalized anxiety disorder and depression revealed plasma concentrations of both amitriptyline and nortriptyline. In humans, the tricyclic antidepressant (TCA) tertiary amines imipramine and amitriptyline are typically metabolized by demethylation to the secondary active metabolites desipramine and nortriptyline, respectively. However, to our knowledge, methylation of secondary amine TCAs has been reported in only one case report of nortriptyline overdose and in two studies involving desipramine. In a retrospective analysis of patients from five Veterans Affairs medical centers, the rate of methylation of desipramine and nortriptyline was 8.9 % (five of 56 patients) and 14.6% (36 of 247), respectively. Possible explanations for methylation include genetic polymorphisms in cytochrome P450 metabolizing enzymes, polymorphism of amine N-methyltransferase enzyme, drug-drug interactions, smoking, and alcohol consumption. However, the mechanism by which methylation occurs is unclear and warrants further investigation. Awareness of the phenomenon could help in discouraging repeated laboratory tests and unnecessary adjustments of drug therapies, resulting in cost savings and better patient outcomes.

Aged, 80 and over↗

PubMedDate not supplied

Effect of desipramine during infancy and preweanling on dorsal striatal dopamine D1 and D2 receptor binding in adolescence in the rat.

Desipramine, a monoamine uptake inhibiting antidepressant, was given once a day sc from the 6th to the 22nd postnatal days, which is during infancy and preweanling in ontogenesis, to rats and its effects on dorsal striatal dopamine D1 and D2 receptor binding in adolescence were examined. The rats were decapitated, their dorsal striata were dissected on approximately the 34th postnatal day, and the maximal densities (Bmax) and affinities (Kd) of dopamine D1 and D2 receptors were assayed using [3H] SCH 23390 and [3H] spiperone as ligands. Desipramine did not affect the densities or affinities of dopamine D1 or D2 receptor binding, and tended to increase the D1/D2 density ratio. The Bmax of dopamine D2 receptors was higher in male than in female rats (p<0.01), the D1/D2 Bmax ratio tended to be lower in male than in female rats (p<0.07), and the Kd for D1 receptors tended to be lower in male than in female rats (p<0.05). There was no interaction between treatment and gender. We conclude that desipramine given at infancy and preweanling increases the susceptibility of adolescent rats to behavioral effects of dopamine agonists with an optimal, and relatively high SCH 23390/spiperone binding site density ratio. Furthermore, gender differences in dorsal striatal spiperone binding site densities, SCH 23390/spiperone density ratio, and SCH 23390 affinities may render male rats more vulnerable than female rats to expression of excessive stereotyped behavior.

Adrenergic Uptake Inhibitors↗

PubMedDate not supplied

[Comparative study of hemodynamic effects of antidepressants (tetrindole and desipramine) during immobilization stress in hypertensive rats].

Tetrindole (a tetracyclic antidepressant, reversible MAO inhibitor of the A type) and desipramine (a tricyclic antidepressant, nonselective inhibitor of the reverse catecholamine trapping) produce opposite hemodynamic effects in stroke-prone hypertensive rats (SHR-SP): tetrindole reduced, whereas desipramine increased, the heart rate and arterial pressure. Under the acute immobilization stress conditions in SHR-SP, tetrindole inhibited development of the post-stressor tachycardia, while desipramine did not change the heart rate and increased the arterial pressure.

Animals↗

PubMed2001

Comparison of desipramine and cognitive/behavioral therapy in the treatment of elderly outpatients with mild-to-moderate depression.

The authors evaluated the efficacy of desipramine-alone, vs. cognitive/behavioral therapy-alone (CBT) vs. a combination of the two, for the treatment of depression in older adult outpatients. Patients (N=102) meeting criteria for major depressive disorder were randomly assigned to one of these three treatments for 16 to 20 therapy sessions. All treatments resulted in substantial improvement. In general, the CBT-Alone and Combined groups had similar levels of improvement. In most analyses, the Combined group showed greater improvement than the Desipramine-Alone group, whereas the CBT-Alone group showed only marginally better improvement. The combined therapies were most effective in patients who were more severely depressed, particularly when desipramine was at or above recommended stable dosage levels. The results indicate that psychotherapy can be an effective treatment for older adult outpatients with moderate levels of depression.

Aged↗

PubMed2004

'Compulsive' lever-pressing in rats is attenuated by the serotonin re-uptake inhibitors paroxetine and fluvoxamine but not by the tricyclic antidepressant desipramine or the anxiolytic diazepam.

Rats undergoing extinction of lever-pressing for food after the attenuation of an external feedback for this behavior, exhibit excessive lever-pressing unaccompanied by an attempt to collect a reward, which may be analogous to the excessive and unreasonable behavior seen in obsessive-compulsive disorder (OCD). Given that one of the most salient features of OCD is its selective response to treatment with serotonin re-uptake inhibitors (SRIs), the present study compared the effects of the SRIs paroxetine and fluvoxamine on compulsive lever-pressing, with those of the tricyclic antidepressant, desipramine, and the benzodiazepine, diazepam, which are not effective in the treatment of OCD. Paroxetine (1-15 mg/kg) and fluvoxamine (10-20 mg/kg) dose-dependently reduced the number of compulsive lever-presses and the number of lever-presses followed by an attempt to collect a reward; desipramine (5-15 mg/kg) dose-dependently reduced only the number of lever-presses followed by an attempt to collect a reward; diazepam (2-10 mg/kg) did not affect either type of lever-pressing, except for the highest dose (10 mg/kg), which almost completely abolished lever-press responding. When administered in an extinction session not preceded by signal attenuation, paroxetine, fluvoxamine and desipramine affected only the number of lever-presses followed by an attempt to collect a reward, whereas diazepam (4-8 mg/kg) decreased both types of lever-presses. The present findings strengthen the suggestion that compulsive lever-pressing may serve to model compulsive behavior in OCD, and lends the model predictive validity.

Animals↗

PubMed1992

Increased pulse and blood pressure associated with desipramine treatment of bulimia nervosa.

The cardiovascular effects of desipramine were assessed in 74 young women with bulimia nervosa participating in a 6-week double-blind, placebo-controlled study. Desipramine treatment was associated with significant increases in pulse, reclining systolic and diastolic blood pressures, and orthostatic hypotension. These effects were clearly evident in the first week of treatment and remained relatively unchanged during the subsequent 5 weeks. The mean increases in reclining systolic and diastolic pressures were approximately 10 mm Hg. Data from 16 patients treated for an additional 2 months indicated that most of the effects of desipramine on blood pressure diminished over time, whereas the effects on pulse persisted. These results differ from the commonly expected cardiovascular effects of tricyclic anti-depressants in adults. Evidence from the current study and from other reports suggests that the cardiovascular effects of tricyclic antidepressants are age-dependent.

Adolescent↗

PubMed1991

Clinical and neuropsychological effects of desipramine in children with attention deficit hyperactivity disorder.

Desipramine is a tricyclic antidepressant with demonstrated efficacy for some children with attention deficit hyperactivity disorder (ADHD). In this controlled study, clinical improvement was noted in a group of 12 ADHD children. There also were neuropsychological effects associated with desipramine treatment: a small but significant decline in motor performance and an improvement in long-term verbal memory. The decline in motor performance may be of only limited clinical significance, but it is an effect that desipramine seems to share with other tricyclic antidepressants. The improvement in memory performance is an effect it shares with the psychostimulants.

Affect↗

PubMed1990

Desipramine blocks stress-induced prolactin release in rats: role of central beta-2 adrenoceptors.

1. The present study was designed to examine the relationship between beta-adrenoceptors and the enhanced, sustained prolactin secretion induced by immobilization stress in rats. 2. Chronic administration of desipramine (15 mg kg-1 day-1, intraperitoneally) for 7 days, a procedure that desensitizes central beta-adrenoceptors, partially inhibits stress-induced prolactin release. 3. Intracerebroventricular administration of the beta-2 adrenoceptor agonist salbutamol (1 microgram/rat) to rats pretreated with desipramine for 7 days, 15 min before immobilization, significantly relieved the inhibition by desipramine 5 and 10 min after the initiation of stress but the effect was not demonstrable after 20 and 40 min. 4. We conclude that beta-2 adrenoceptors play a role in the control of prolactin release in response to stress.

Albuterol↗

PubMed1989

[Ethanol-induced discriminative stimulus properties in inbred rats with reference to aspirin, indomethacin and desipramine].

It is known that ethanol (EtOH) possesses discriminative stimulus (DS) effects, but there has been no report on the effects of aspirin, indomethacin and desipramine on the DS properties of EtOH. Lewis (LEW) and Fischer 344 (F344) rats weighing approximately 80% of free-fed animals were used. In the training process, EtOH (600 and 1200 mg/kg) or saline was administered i.p. once a day 5 min prior to beginning of the session according to the following sequence: EtOH-EtOH-saline-saline, under a fixed ratio ten (FR10) schedule. Discriminative test was performed in each animal after the discriminative response had achieved both the two criteria: (1) First Food Pellet (FFP) was below 12 responses and (2) the correct response rate was above 80%. There was no difference in session number to get to the criteria in the discrimination process between LEW and F344. Pentobarbital (PBA) well generalized to EtOH in both strains. The EtOH dose for 50% correct responses (FD50) was lower in F344 than in LEW. However, the ED50 for PBA was lower in LEW than in F344. There may be differences in sensitivity to EtOH and PBA. Dose response curve was not affected by pretreatment with aspirin, indomethacin and desipramine. These results suggest that aspirin, indomethacin and desipramine may not markedly affect in EtOH discriminative stimulus effects in LEW and F344 rats.

Animals↗

PubMed1988

Relapse to cocaine abuse after initiating desipramine treatment.

Three cocaine abusers who had been abstinent for one to six months relapsed to cocaine use soon after beginning desipramine hydrochloride therapy. The antidepressant treatment was begun for different reasons in each case. All three patients developed what has been termed the early tricyclic jitteriness syndrome. This reaction may have stimulated conditioned craving for cocaine because of the similarity between this syndrome and cocaine intoxication. Since desipramine is being used to reduce cocaine craving, it is important to recognize this paradoxical increase in craving as a potential adverse effect of desipramine.

Adult↗

PubMed1988

Cocaine-elicited mydriasis in the rat: pharmacological comparison to clonidine, D-amphetamine and desipramine.

Agents known to influence adrenergic function were examined for their mydriatic effects in urethane-anesthetized rats. Both the direct acting adrenergic agonist, clonidine, and the "indirect" acting agonists, cocaine, desipramine and amphetamine elicited mydriatic responses. The polar alpha-2 adrenoceptor agonist, 4-hydroxyclonidine, did not elicit a mydriatic response when administered systemically; however, it did produce a pronounced mydriatic response when administered i.c.v. Inasmuch as the selective lipophilic alpha-2 adrenoceptor antagonist, yohimbine, but not the polar alpha adrenoceptor antagonist, phentolamine, reversed the mydriatic effects of clonidine and cocaine, these data suggest that centrally located alpha-2 adrenoceptors elicit the above mydriatic response. The direct acting alpha-2 adrenoceptor agonists, clonidine (i.v.) and 4-hydroxyclonidine (i.c.v.), were the most efficacious of the agents studied in eliciting the mydriatic response. The indirect acting agents, amphetamine, desipramine and cocaine, were less efficacious. The rank order potency (ED-50) of these drugs was as follows: clonidine greater than desipramine greater than cocaine = amphetamine. The mydriatic effects of cocaine were attenuated by yohimbine and reserpine pretreatments. In addition, the local anesthetic, procaine, and the polar cocaine analog, cocaine methiodide, were significantly less efficacious than cocaine. These results suggest that cocaine elicits mydriasis by indirectly acting at central and postsynaptically located alpha-2 adrenoceptors.

Animals↗

PubMedDate not supplied

Desipramine antagonizes clonidine-induced suppression of dominance in rats: possible involvement of amygdaloid nuclei.

Bilateral microinjections of clonidine into the medial or basal amygdaloid nuclei suppressed the dominance behavior in rats competing for food. Desipramine given in five repeated daily doses antagonized clonidine effect. On the other hand suppression of dominance induced by clonidine given bilaterally into the cortical amygdaloid nucleus was resistant to desipramine treatment. The result suggests that the former nuclei are important target areas for clonidine-desipramine interaction at social interaction behavioral level.

Amygdala↗

PubMedDate not supplied

[Preliminary results of a double-blind study between rolipram and desipramine in hospitalized patients with major depressive symptoms].

Rolipram facilitates the postsynaptic neurotransmission of NA through a completely new mechanism of action, namely, an inhibition of the inactivation of the second messenger (the cyclic AMP) by phosphodiesterase. In the present study, Rolipram is compared to a classical tricyclic antidepressant which facilitates the NA transmission through an inhibition of its presynaptic reuptake: Desipramine. Preliminary results on 12 Rolipram patients vs. 9 Desipramine patients indicate that Rolipram has an antidepressant potency comparable to Desipramine with less anticholinergic and hypotensive side effects. This study also illustrates that a 14-factor AMDP profile gives much more information than a single total score such as the Hamilton score.

Adolescent↗

PubMed1979

A double-blind comparative study of desipramine hydrochloride and diazepam in the control of mixed anxiety/depression symptomatology.

The comparative therapeutic effects of desipramine hydrochloride and diazepam on the various symptoms of depression and anxiety were evaluated in a double-blind, parallel 4 week study of 53 psychoneurotic outpatients who manifested moderate-to-severe depression and anxiety. The median daily dose for the desipramine treated group was 150 mg; for the diazepam treated group, 20 mg. Patients who received desipramine scored significantly better than diazepam treated patients on 26 of the total of 51 variables derived from The Hamilton Psychiatric Rating Scale for Depression, The Hamilton Psychiatric Rating Scale for Anxiety, and 2 clinical global impressions. Patients who received diazepam scored significantly better on 1 variable, an item pertaining to sleep.

Adjustment Disorders↗